Molecular mechanisms of mutation will be investigated in coliphages T4 and lambda. A model of misrepair mutagenesis which holds that mutations occur only when induced progeny-strand gaps in DNA overlap will be tested by measuring the mutagenicity of ultraviolet-induced lesions confined to a single strand of the DNA of phage lambda. A search will be initiated for an enzyme (such as DNA terminal transferase) induced by phage T4 infection which can aid untemplated bases in such gaps opposite to the parental strand lesions. The role of the viral DNA polymerase in misrepair mutagenesis will be assessed in phage T4 by measuring the effects of mutator and antimutator alleles of the polymerase gene on rates of ultraviolet-induced mutagenesis. A model of heat mutagenesis in phage T4 which holds that guanosine is converted to the cytosine analogue neoguanosine will be tested by synthesizing deoxyneoguanosine triphosphate, incorporating it into defined deoxyribonucleotide polymers, and testing their ability to direct the incorporation of cytosine in vitro DNA polymerase reaction. Repair enzymes capable of excising such residues will be sought in a variety of organisms.